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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3439-3446
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Fc RIIA requires a Gi-dependent pathway for an efficient
stimulation of phosphoinositide 3-kinase, calcium mobilization, and
platelet aggregation
Marie-Pierre Gratacap,
Jean-Pascal Hérault,
Cécile Viala,
Ashraf Ragab,
Pierre Savi,
Jean-Marc Herbert,
Hugues Chap,
Monique Plantavid, and
Bernard Payrastre
From Institut Fédératif de Recherche en
Immunologie Cellulaire et Moléculaire, Université Paul
Sabatier and Centre Hospitalo - Universitaire de Toulouse, Institut
National de la Santé et de la Recherche médicale,
Unité 326, Hôpital Purpan, 31059 Toulouse Cedex, France;
and Sanofi-Synthelabo, Route d'Espagne, 31036 Toulouse Cedex, France.
Fc RIIA, the only Fc receptor present in platelets, is
involved in heparin-associated thrombocytopenia (HIT). Recently,
adenosine diphosphate (ADP) has been shown to play a major role in
platelet activation and aggregation induced by FcRIIA cross-linking
or by sera from HIT patients. Herein, we investigated the mechanism of
action of ADP as a cofactor in FcRIIA-dependent platelet activation, which is classically known to involve tyrosine kinases. We first got
pharmacologic evidence that the ADP receptor coupled to Gi was required
for HIT sera or FcRIIA clustering-induced platelet secretion and
aggregation. Interestingly, the signaling from this ADP receptor could
be replaced by triggering another Gi-coupled receptor, the
 2A-adrenergic receptor. ADP scavengers did not significantly affect the tyrosine phosphorylation cascade initiated by FcRIIA cross-linking. Conversely, the Gi-dependent signaling pathway, initiated either by ADP or epinephrine, was required for
FcRIIA-mediated phospholipase C activation and calcium mobilization. Indeed, concomitant signaling from Gi and FcRIIA itself was
necessary for an efficient synthesis of phosphatidylinositol
3,4,5-trisphosphate, a second messenger playing
a critical role in the process of phospholipase C2 activation.
Altogether, our data demonstrate that converging signaling pathways
from Gi and tyrosine kinases are required for platelet secretion and
aggregation induced by FcRIIA.
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